Background: To date, although several long noncoding RNAs (lncRNAs) are reported to regulate hepatocellular carcinoma (HCC) development, their relationship still remains elusive. ASB16-AS1 is a poorly researched novel lncRNA. We aimed to investigate its function in HCC progression.
Methods: qRT-PCR and in situ hybridization (ISH) were used to analyze ASB16-AS1 expression in HCC tissues. CCK8, Edu incorporation and colony formation were used to determine cell proliferation. Transwell assay was used to examine migration and invasion. Luciferase reporter assay was used to analyze the interactions among ASB16-AS1, miR-1827 and FZD4.
Results: Bioinformatics analysis identified ASB16-AS1 was overexpressed in HCC tissues, which was further validated by qRT-PCR and in situ hybridization (ISH). Besides, ASB16-AS1 was demonstrated to be a potential indicator for HCC prognosis. Functional studies showed ASB16-AS1 knockdown attenuated proliferation, migration and invasion of HCC cells. Mechanistically, ASB16-AS1 directly interacted with miR-1827 and promoted FZD4 expression by sponging miR-1827. Overexpressed FZD4 eventually activated Wnt/β-catenin pathway and contributed to HCC progression.
Conclusion: Our work is the first to identify ASB16-AS1 as an oncogene that enhances HCC progression by modulating miR-1827/FZD4/Wnt/β-catenin pathways.
Keywords: lncRNA, HCC, ASB16-AS1, miR-1827, FZD4